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Because physical demands are surging in football (soccer, USA), clubs are more and more seeking players who have a high capacity to perform repeated intense exercise. High-intensity interval training (HIIT), comprising exercise performed at intensities near or exceeding the capacity of aerobic energy systems, effectively enhances the physical conditioning of players. But given that HIIT imposes high loads, it increases the risk of overload-associated match performance decline and injury. This makes some coaches inclined to conduct HIIT in the weeks leading up to the season and during the season. Therefore, the challenge is how to optimize and dose HIIT during these phases, as they can be decisive. Studies have highlighted the utility of conducting periods of intensified training to overcome the risk of overload while at the same time enhancing performance. During intensified training periods of typically a few weeks, intensity is increased by enlarging the amount of HIIT, for example, aerobic high-intensity training or speed endurance training, while volume at low-to-moderate intensity is significantly reduced. The outcome depends on training composition and prescription-most notably, intensity and duration of bouts and recovery. When work intervals are prescribed for a few minutes at intensities > 90% heart rate max (i.e., aerobic high-intensity training), then beneficial adaptations pertaining to aerobic power and capacity are apparent. But when work intervals are conducted at much higher intensities, as all-out efforts or sprinting of typically 10- to 40-s duration with longer recovery periods (i.e., speed endurance training), beneficial adaptations pertaining to anaerobic energy systems, ion handling, and fatigue resilience are commonly observed. In this review, we discuss the utility of conducting intensified training periods to enhance performance in elite football players during the late preparation phase and competitive season.

Intense interval exercise training has been shown to improve performance and health of untrained and trained people. However, due to the exercise intensity causing high‐perceived exertion, the participants often do not wish to continue the training. The 10‐20‐30 training concept consists of low intensity for 30 s, 20 s at a moderate pace, and then 10 s with high intensity either running or cycling. A 10‐20‐30 training session consist of two to four 5‐min blocks. The 10‐20‐30 training improved fitness and performance as well as lowered blood pressure and body fat of both untrained and trained individuals even with a significant reduction in the training volume. Similarly, hypertensive, diabetic, and asthmatic patients lowered body fat, improved fitness, and performance during a 10‐20‐30‐training intervention period. In addition, hypertensive patients reduced systolic and diastolic blood pressure markedly with the 10‐20‐30 training twice a week for 8 weeks. Diabetic patients lowered long‐term blood sugar (HbA1c), which did not occur with moderate‐intensity exercise training. Furthermore, asthmatic patients improved their control of asthma and asthma‐related quality of life with the 10‐20‐30 training. The adherence for the patient groups was high (>80%), and no adverse events were reported. Thus, the 10‐20‐30 training seems to be time efficient and feasible for untrained and trained individuals as well as patients and may be used in the prevention and treatment of noncommunicable diseases. Highlights What is already known? Aerobic moderate‐intensity exercise training has been shown to improve fitness and health of untrained individuals. Intense exercise training has been shown to benefit some patient groups, but many patients are struggling with the training due to the strenuous effort experienced during training. Untrained individuals and patients have difficulties to find time and motivation to do physical activities. What are the findings? The 10‐20‐30 training is a new training modality, which has greater benefits than aerobic moderate‐intensity training, and is a more time‐efficient way to improve performance and health even in trained people. The 10‐20‐30 training reduces blood pressure and body fat in untrained and already trained people even with lowered training volume. The 10‐20‐30 training is feasible for hypertensive, diabetic, and asthmatic patients, who with the 10‐20‐30 training are reducing blood pressure, improve long‐term blood sugar management, and lower symptoms of asthma, respectively.

Over the past 10 years, researchers have studied the effects of recreational football training as a health-promoting activity for participants across the lifespan. This has important public health implications as over 400 million people play football annually. Results from the first randomised controlled trial, published in the BJSM in January 2009, showed that football increased maximal oxygen uptake and muscle and bone mass, and lowered fat percentage and blood pressure, in untrained men, and since then more than 70 articles about football for health have been published, including publications in two supplements of the Scandinavian Journal of Medicine and Science in Sports in 2010 and 2014, prior to the FIFA World Cup tournaments in South Africa and Brazil. While studies of football training effects have also been performed in women and children, this article reviews the current evidence linking recreational football training with favourable effects in the prevention and treatment of disease in adult men.

Exercise is an effective strategy in the prevention and treatment of metabolic diseases. Alterations in the skeletal muscle proteome, including post-translational modifications, regulate its metabolic adaptations to exercise. Here, we examined the effect of high-intensity interval training (HIIT) on the proteome and acetylome of human skeletal muscle, revealing the response of 3168 proteins and 1263 lysine acetyl-sites on 464 acetylated proteins. We identified global protein adaptations to exercise training involved in metabolism, excitation-contraction coupling, and myofibrillar calcium sensitivity. Furthermore, HIIT increased the acetylation of mitochondrial proteins, particularly those of complex V. We also highlight the regulation of exercise-responsive histone acetyl-sites. These data demonstrate the plasticity of the skeletal muscle proteome and acetylome, providing insight into the regulation of contractile, metabolic and transcriptional processes within skeletal muscle. Herein, we provide a substantial hypothesis-generating resource to stimulate further mechanistic research investigating how exercise improves metabolic health.

The aim of the present study was to examine the role of PGC-1α in intensity dependent exercise and exercise training-induced metabolic adaptations in mouse skeletal muscle. Whole body PGC-1α knockout (KO) and littermate wildtype (WT) mice performed a single treadmill running bout at either low intensity (LI) for 40 min or moderate intensity (MI) for 20 min. Blood and quadriceps muscles were removed either immediately after exercise or at 3h or 6h into recovery from exercise and from resting controls. In addition PGC-1α KO and littermate WT mice were exercise trained at either low intensity (LIT) for 40 min or at moderate intensity (MIT) for 20 min 2 times pr. day for 5 weeks. In the first and the last week of the intervention period, mice performed a graded running endurance test. Quadriceps muscles were removed before and after the training period for analyses. The acute exercise bout elicited intensity dependent increases in LC3I and LC3II protein and intensity independent decrease in p62 protein in skeletal muscle late in recovery and increased LC3II with exercise training independent of exercise intensity and volume in WT mice. Furthermore, acute exercise and exercise training did not increase LC3I and LC3II protein in PGC-1α KO. In addition, exercise-induced mRNA responses of PGC-1α isoforms were intensity dependent. In conclusion, these findings indicate that exercise intensity affected autophagy markers differently in skeletal muscle and suggest that PGC-1α regulates both acute and exercise training-induced autophagy in skeletal muscle potentially in a PGC-1α isoform specific manner.

Background: Hypertension is a significant public health issue, particularly in individuals with comorbidities such as COPD and T2DM, which exacerbate cardiovascular risk and impair quality of life. While physical activity is an effective intervention for reducing blood pressure and improving health markers, conventional therapies often lack the social and psychological benefits of team sports. Team sports conducted as small-sided games provide a dynamic, engaging approach that combines physical, social, and psychological advantages, making them particularly suitable for individuals with complex chronic conditions. Methods: This non-randomized intervention study involved twenty-eight hypertensive patients, including 16 individuals with type 2 diabetes mellitus (T2DM) (8 men and 8 women) and 12 with chronic obstructive pulmonary disease (COPD) (7 men and 5 women). Participants engaged in a training program, primarily consisting of team sports (floorball and cone ball), at a municipal health center twice a week for 12 weeks. Results: The intervention led to a significant reduction in systolic blood pressure (p = 0.006), with patients with COPD and T2DM showing decreases of 9.6 ± 12.7 mmHg and 12.4 ± 19.0 mmHg, respectively. Additionally, the time to complete the 2.45 m “Up and Go” test improved significantly (p < 0.001), with both COPD (p = 0.011) and T2DM (p = 0.005) patients demonstrating notable improvements. However, no significant changes were observed in body mass, chair stand performance, five-repetition sit-to-stand test, handgrip strength, or diastolic blood pressure following the intervention. Conclusions: Team sports training conducted in a municipality health center is effective in lowering blood pressure and improving functional capacity in hypertensive COPD and T2DM patients.

Moderately trained male subjects (mean age 25 years; range 19–33 years) completed an 8‐week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30‐sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts. A single exercise bout seems to increase autophagosome number, and exercise training seems to increase the capacity for autophagy and mitophagy regulation in human skeletal muscle. In addition, the present findings provide evidence that these effects are unaffected by interspersed sprint bouts, although regulation of some autophagy markers appear to be inhibited by short lasting high‐intensity bouts.

This study is the first to determine how hypoxia affects human muscle fatigue kinetics and metabolic perturbations during intense dynamic exercise. Using randomized, single-blinded crossover designs, three trials of two-legged knee extensions were performed under hypoxic (HYP, FiO₂ 0.135) and normoxic (NOR) conditions. Trial 1 ( n  = 8): quadriceps femoris twitch force (F tw ) was measured before, during, and after 4 min intense exercise followed by exhaustive exercise. Maximal voluntary contraction (MVC) was measured pre- and post-exercise. Trial 2 ( n  = 8): muscle lactate and pH were determined before and after 4 min intense exercise. Trial 3 ( n  = 6): blood was sampled frequently from the femoral artery and vein during intense exhaustive exercise. Dynamic F tw decreased more ( P  < 0.05) in HYP from 60s of exercise and onwards. After 4 min, isometric F tw decreased more ( P  < 0.05) in HYP, whereas MVC was similar between conditions. At exhaustion, isometric F tw and MVC were similar between conditions despite HYP exercise time being 55 ± 17% of NOR ( P  < 0.01). Muscle lactate and pH in- and decreased more ( P  < 0.001), respectively, after 4 min in HYP. Exercise-induced blood metabolites disturbances were largely unaffected by hypoxia. Conclusively, moderate hypoxia accelerated muscular fatigue from 60s and onwards. Hypoxia caused higher muscle but not blood lactate and H + accumulation rates.

Exercise training is a cornerstone in reducing blood pressure (BP) and muscle sympathetic nerve activity (MSNA) in individuals with essential hypertension. High-intensity interval training (HIIT) has been shown to be a time efficient alternative to classical continuous training in lowering BP in essential hypertension, but the effect of HIIT on MSNA levels has never been investigated. Leg MSNA responsiveness to six weeks of HIIT was examined in fourteen hypertensive men (HYP; age: 62±7 years, night time BP: 136±12/83±8 mmHg, BMI: 28±3 kg/m2), and ten age-matched normotensive controls (NORM; age: 60±8 years, night time BP: 116±2/68±4 mmHg and BMI: 27±3 kg/m2). Before training, MSNA levels were not different between HYP and NORM (burst frequency (BF): 41.0±10.3 vs. 33.6±10.6 bursts/min and burst incidence (BI): 67.5±19.7 vs. 64.2±17.0 bursts/100 heart beats, respectively). BF decreased (P<0.05) with training by 13 and 5 % in HYP and NORM, respectively, whereas BI decreased by 7% in NORM only, with no difference between groups. Training lowered (P<0.05) night-time mean arterial- and diastolic BP in HYP only (100±8 vs. 97±5, and 82±6 vs. 79±5 mmHg, respectively). The change in HYP was greater (P<0.05) compared to NORM. Training reduced (P<0.05) body mass, visceral fat mass and fat percentage similarly within- and between groups, with no change in fat free mass. Training increased (P<0.05) V̇O2-max in NORM only. Six weeks of HIIT lowered resting MSNA levels in age-matched hyper- and normotensive men, which was paralleled by a significant reduction in BP in the hypertensive men.

In order to better understand the specificity of training adaptations, we compared the effects of two different anaerobic training regimes on various types of soccer-related exercise performances. During the last 3 weeks of the competitive season, thirteen young male professional soccer players (age 18.5±1 yr, height 179.5±6.5 cm, body mass 74.3±6.5 kg) reduced the training volume by ~20% and replaced their habitual fitness conditioning work with either speed endurance production (SEP; n = 6) or speed endurance maintenance (SEM; n = 7) training, three times per wk. SEP training consisted of 6-8 reps of 20-s all-out running bouts followed by 2 min of passive recovery, whereas SEM training was characterized by 6-8 x 20-s all-out efforts interspersed with 40 s of passive recovery. SEP training reduced (p<0.01) the total time in a repeated sprint ability test (RSAt) by 2.5%. SEM training improved the 200-m sprint performance (from 26.59±0.70 to 26.02±0.62 s, p<0.01) and had a likely beneficial impact on the percentage decrement score of the RSA test (from 4.07±1.28 to 3.55±1.01%) but induced a very likely impairment in RSAt (from 83.81±2.37 to 84.65±2.27 s). The distance covered in the Yo-Yo Intermittent Recovery test level 2 was 10.1% (p<0.001) and 3.8% (p<0.05) higher after SEP and SEM training, respectively, with possibly greater improvements following SEP compared to SEM. No differences were observed in the 20- and 40-m sprint performances. In conclusion, these two training strategies target different determinants of soccer-related physical performance. SEP improved repeated sprint and high-intensity intermittent exercise performance, whereas SEM increased muscles' ability to maximize fatigue tolerance and maintain speed development during both repeated all-out and continuous short-duration maximal exercises. These results provide new insight into the precise nature of a stimulus necessary to improve specific types of athletic performance in trained young soccer players.